Abstract
Our previous study found that 17β-estradiol (E2) suppresses primordial follicle activation and growth in cultured mouse ovaries. In this study, we administered tamoxifen, an estrogen receptor antagonist, into the abdominal cavity of mice to clarify the relationship between primordial follicle activation and the physiological concentration of E2 in mouse ovaries. The results showed that tamoxifen promoted primordial follicle activation. Administration of tamoxifen promoted degradation of the extracellular matrix surrounding primordial follicles in the ovaries. Furthermore, tamoxifen decreased the expression of stefin A, an inhibitor of cathepsins that digest some proteins and extracellular matrix, in the ovaries. Mechanical stress produced by the extracellular matrix reportedly suppresses the activation of primordial follicles. The collective results show that tamoxifen can promote primordial follicle activation through the degradation of the extracellular matrix surrounding primordial follicles. Our results indicate that E2 suppresses primordial follicle activation in vivo and that tamoxifen may be useful as a therapeutic agent against infertility.
Highlights
Ovarian folliculogenesis starts with the recruitment of dormant primordial follicles into the growing follicle pool to form a primary, secondary, preantral follicle, and a preovulatory antral follicle [1]
We investigated the relationship between primordial follicle activation (PFA) during the estrous cycle and estradiol concentration in the serum and ovarian tissue to clarify the physiological mechanism of PFA
There was no significant change in the rate of activated primordial follicles around antral follicles in all stages of the estrous cycle (Fig. 4b and Supplementary Table 4; proestrus: control: 0.11 ± 0.1, tamoxifen: 0.13 ± 0.08; estrus: control: 0.14 ± 0.06, tamoxifen: 0.12 ± 0.08; metestrus: control: 0.16 ± 0.04, tamoxifen: 0.15 ± 0.06; diestrus: control: 0.15 ± 0.04, tamoxifen: 0.16 ± 0.04). These results showed that tamoxifen promoted PFA except for the primordial follicles around the antral follicles
Summary
Ovarian folliculogenesis starts with the recruitment of dormant primordial follicles into the growing follicle pool to form a primary, secondary, preantral follicle, and a preovulatory antral follicle [1]. Loss of estrogen receptor β (ESR2), the predominant estrogen receptor in the ovary, leads to primordial follicle activation (PFA) [22]. These results suggest that E2 controls PFA.
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